Theories of Aging Based On Random EventsTheories on why we age may be divided into those based on random events, external or environmental influences -- and those that are programmatic, genetically and biologically driven. Of course, reality may include a combination of these factors. This page looks at the major random-events based theories. The main random-event theories are:
Of these, only the first three have much evidence supporting them. The cross-linking theory of aging is based on the observation that with age, our proteins, DNA and other structural molecules develop inappropriate attachments or cross-links to one another. Such age related features as skin wrinkles and cataracts have been attributed to cross-linking. The 'Wear and Tear' theory is a bit misleading, as most of the damage occurs at the cellular level, not what we normally think of when talking of wear and tear: The DNA that makes up our genes sustains repeated damage from toxins, radiation and ultraviolet light. Some genetic damage gets repaired, but the repairs are not always perfect, and errors accumulate. The free radical theory has some experimental support, though results have not been as irrefutable as those from caloric restriction. Free radicals are one of the toxic byproducts of normal cell metabolism. Natural substances within our cells (e.g., antioxidants) sop up and neutralize the dangerous free radicals. But those free radicals that escape this cleanup process can damage DNA, proteins and mitochondria. Large amounts of anti-oxidants have been shown to extend animal lifespans, but some argue they also lead to reduced caloric intake, and that the observed effect is due to caloric restriction. The 'Rate of Living' theory doesn't really have much scientific support and is probably not much of a factor in lifespan. 'Somatic Mutations' may play some role in aging, but it is unlikely to be very significant. |
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